The NA content in the heart was not measured but it is likely to be small at least at the 10-day period. It is known that three days after chemical sympathectomy NA content is only 7% of normal value [6]. Second, the development of adrenoceptor supersensitivity in the transplanted heart was demonstrated clearly with enhanced heart rate responses to NA or propranolol (at Day 10) [1]. As dennervation sensitization increases the arrhythmia susceptibility [6], it is thus possible that, in the presence of receptor supersensitivity, adrenergic activation occurs by either increase in circulating catecholamines and possibly local release of residual NA, which might still have been sufficient to contribute to arrhythmia development.
Role of sympathoadrenergic mechanisms in arrhythmogenesis
Xiao-Jun Du* and Anthony M. Dart
Baker Medical Research Institute, Melbourne, Victoria, Australia
Cardiovascular Research 1999 43(4):832-834;
The heart rate and systolic blood pressure de-
creased significantly after T2-T3ganglionectomy.
A prolonged QT interval was also recorded (p<
0.05). A few minutes later after the operation
bradycardia occurred in 4 rats in the sympathec-
tomy group. The heart rate distributions were
listed in Figure 3.
The decrease in systolic and diastolic blood
pressure was insignificant after the operation in the
control group (p> 0.05). The decrease was signifi-
cant in the sympathectomy group.
Our study also, it was revealed that
sympathectomy significantly prolonged the QT in-
terval.
Surgeons should be aware of adverse effects such as bradycardia during thoracic
sympathectomy. This study suggested that careful monitoring was required during thoracic sym-
pathectomy and early postoperative period.
Orhan YÜCEL, MD
GATA, Department of
Thoracic Surgery, Ankara,
TÜRKİYE/TURKEY
"suppressor T cells through an immune-privileged site
requires an intact sympathetic nervous system."
Journal of Neuroimmunology Volume 147, Issues 1-2, February 2004, Pages 87-90
These experiments indicate that an inflammatory response is not likely to be responsible for sympathectomy-induced immune alterations, eliminating a potential confounding factor in interpreting sympathectomy studies.
Brain, behavior and immunity ISSN 0889-1591
2002, vol. 16, no1, pp. 33-45 [13
CALLAHAN Tracy A. ; MOYNIHAN Jan A. ;
These results support an association between CAN (cardiovascular autonomic neuropathy) and increased risk of mortality. The stronger association observed in studies defining CAN by the presence of two or more abnormalities may be due to more severe autonomic dysfunction in these subjects or a higher frequency of other comorbid complications that contributed to their higher mortality risk. Future studies should evaluate whether early identification of subjects with CAN can lead to a reduction in mortality.
- Raelene E. Maser, PHD1,
- Braxton D. Mitchell, PHD2,
- Aaron I. Vinik, MD, PHD3 and
- Roy Freeman, MD4
"Cardiovascular autonomic neuropathy (CAN) is the most prominent focus because of the life-threatening consequences and the availability of direct tests of cardiovascular autonomic function.. .CAN results from damage due to the autonomic nerve fibers that innervate the heart and blood vessels and results in abnormalities in heart rate control and vascular dynamics.
Reduced heart variation is the earliest indicator of CAN."
"CAN is the most studied and clinically important form of DAN. Meta-analyses of published data demonstrate that
reduced cardiovascular autonomic function as measured by heart rate variability (HRV) is strongly associated with an increased risk of silent myocardial ischemia and mortality. The determination of the presence of CAN is usually based on a battery of autonomic function tests..."
TECHNICAL REVIEW: Standard of Care - Diabetic Autonomic Neuropathy
Aaron I. Vinik, MD, PHD; Braxton D. Mitchell, PHD
Raelene E. Maser, PHD; Roy Freeman, MD
Epidermal nerve fiber densities were significantly reduced in the skin of all patients, consistent with concomitant small-fiber neuropathies. Perivascular infiltration by T cells and macrophages was demonstrated by immunohistochemistry. All patients experienced neurologic improvement in muscle strength and alleviation of sensory symptoms after immunotherapy with corticosteroids, plasma exchange, or cyclophosphamide. Conclusions: Small-diameter sensory nerves are affected in vasculitis in addition to the well-known effect of vasculitis on large-diameter nerves. Significant inflammatory vasculopathy is present in the skin despite the absence of clinically active vasculitic lesions.
Archives of neurology ISSN 0003-9942 CODEN ARNEAS
2005, vol. 62, no10, pp. 1570-1573 [4 page(s) (article)] (24 ref.)
We measured arterial and venous plasma catecholamines and used laser-Doppler flowmetry to measure cutaneous microcirculatory flow in the sympathectomized and in the intact limbs of 3 patients who had undergone regional sympathectomies. Venous concentrations of norepinephrine, the sympathetic neurotransmitter, exceeded arterial concentrations in the intact limbs--a normal finding--but invariably were less than arterial in the sympathectomized limbs of the same patients, both during baseline conditions and during sympathetic stimulation using tilt, standing and the cold pressor test (mean arteriovenous decrement about 40%). Arterial epinephrine levels exceeded venous levels with or without sympathectomy. Skin microvascular flow rapidly decreased during the cold pressor test and the Valsalva maneuver in the intact but not in the sympathectomized limbs, and spontaneous flow oscillations occurred in the sympathectomized limbs. The results suggest that an arteriovenous increment in plasma norepinephrine reflects local release of norepinephrine from sympathetic nerve endings, whereas removal of circulating catecholamines can occur with or without sympathetic neural impulses. Laser-Doppler flowmetry can measure reflexive sympathetically mediated responses of skin microvascular flow and so can detect sympathetic denervation.
PMID: 3517118 [PubMed - indexed for MEDLINE
Not surprisingly, diminished vasoconstrictor responses, similar to the current findings, have been found
in patients with sympathetic dystrophies [26], dysautomias [27], post-regional sympathectomy [28] and
diabetic neuropathies [11].
Additionally, there have been a few reports of EM patients benefitting from sympathectomy or neurolitic
irreversible blocks of the lumbar sympathetic ganglia [22,23], while others have found the symptoms of EM to
be aggravated by such treatment [24,25], possibly as a result of denervation supersensitivity.
Clinical Science (1999) 96, 507ñ512 (Printed in Great Britain)
Roberta C. LITTLEFORD, Faisel KHAN and Jill J. F. BELCH
University Department of Medicine, Section of Vascular Medicine and Biology, Ninewells Hospital and Medical School,
Dundee DD1 9SY, Scotland, U.K.
Combined with loss of active vasodilation, anhidrosis places tetraplegic patients at risk for hyperthermia. Peripheral Nervous System Disease
With normal aging, thermoregulatory sweat output declines due to peripheral neural and eccrine glandular factors, which vary in degree depending on genetic predisposition and level of physical conditioning.[75] Extensive anhidrosis may also accompany disease of the peripheral nervous system. When exposed to an elevated ambient temperature or physical exercise, these individuals may present with symptoms of heat intolerance, dizziness, weakness, flushing, dyspnea, or palpitations and may be at risk for heat exhaustion and hyperthermia.
Peripheral Neuropathy
Distal anhidrosis, although often subclinical, is detectable by clinical sudomotor testing in many patients with peripheral neuropathy.[76,77] Diabetes mellitus, the most common cause of autonomic neuropathy in the developed world, typically impairs thermoregulatory sweating in a stocking and glove distribution.[78] As the neuropathy progresses, asymmetric truncal anhidrosis or global anhidrosis may develop.[76]
Some immune-mediated neuropathies selectively target the autonomic neuron. Autoimmune autonomic neuropathy typically presents with sicca complex, anhidrosis, gastrointestinal hypomotility, orthostatic hypotension, abnormal pupillary light reflexes, and neurogenic bladder that may be subacute or insidious in onset. Autoantibodies to the ganglionic acetylcholine receptor have been demonstrated in these patients.[29,79,80] Subacute autonomic neuropathy may signal an occult malignancy, most commonly small cell lung carcinoma. The dysautonomia in paraneoplastic autonomic neuropathy can be manifested mainly by cholinergic failure presenting as gastrointestinal dysfunction and anhidrosis.
Hypohidrosis commonly occurs in the autonomic neuropathy associated with Sjögren's syndrome.[83,84] Hypohidrosis also accompanies neuropathies due to amyloidosis, alcoholism, Tangier disease, vasculitis, and Fabry's disease.[85] Focal areas of hypohidrosis may be found in patients with leprosy.[86]
Anhidrosis is a prominent feature of hereditary sensory and autonomic neuropathies type IV and V (congenital insensitivity to pain with anhidrosis), in which absent skin innervation is associated with mutations of the NTRK1 gene encoding the neurotrophic tyrosine kinase receptor type 1.[30]
http://www.medscape.com/viewarticle/473206_3
Nerve conduction studies for large-diameter motor and sensory nerves were normal. This report documents a pure small-fibre sensory neuropathy after prolonged use of linezolid, and the relationship between skin innervation and corresponding neuropathic pain.
Journal of Neurology, Neurosurgery, and Psychiatry 2008;79:97-99
The indications for neurolytic or surgical sympathectomy are uncertain. There is no clear correlation between the degree or duration of pain relief and the actual period of sympathetic blockade and the same patient may show variable responses on different occasionsv (Loh et al 1980). Some patients demonstrate unexpected responses such as contralateral or delayed blocks and some are made worse (Purcell-Jones &Justins 1988, Evans et al 1980, Kleiman 1954)
Neurological Rehabilitation
by R. Greenwood
"All neurological diseases can cause short- and long-term disability..."- Publisher: Psychology Press; New edition edition (February 1, 1997)
- Language: English
- ISBN-10: 0863774849
Ligation injury of the L5/L6 nerve roots in rats produces behavioral signs representative of clinical conditions of neuropathic pain, including tactile allodynia and thermal and mechanical hyperalgesia.
Anesthesiology:
January 1997 - Volume 86 - Issue 1 - pp 196-204
Laboratory Investigation
The injured tissue distal to the ablated segment becomes hypersensitive to
acetylcholine. This can explain why CH may appear very early after
sympathectomy.
All patients except one suffered from compensatory sweating, which was the main cause of patients' dissatisfaction postoperatively. Seventeen percent of the patients (12 of 72 patients) experienced new symptoms of gustatory sweating (facial sweating associated with eating). Twenty-one patients experienced other complications, including pneumothorax, Horner's syndrome, nasal obstruction, and intercostal neuralgia.
CONCLUSION: Transthoracic endoscopic sympathectomy is an effective and simple modality to treat palmar hyperhidrosis. However, all patients need to be warned of the common complications, particularly compensatory hyperhidrosis, before surgery.
by MC Kao -
1998
Neurosurgery:
July 1997 - Volume 41 - Issue 1 - pp 110-115
Some P.G.R. studies in a female subject who had bilateral cervical sympathectomy were described. It was found that sympathectomy abolished P.G.R. and that intra-arterial infusion of acetylcholine evoked marked P.G.R. changes in the sympathectomized limb. These findings support the theory that the P.G.R. is mediated through the cholinergic fibres of the sympathetic nervous system.
Submitted on May 22, 1967
The British Journal of Psychiatry (1968) 114: 639-642. doi: 10.1192/bjp.114.510.639
© 1968 The Royal College of Psychiatrists © 1975 American Heart Association, Inc.
Scandinavian Cardiovascular Journal, Volume
14, Issue
1 1980 , pages 109 - 111
In the majority of 16 non-cardiac and in two angina pectoris patients, unilateral
or bilateral endoscopic transthoracic sympathectomy (method of Kux) was followed
by signs of augmented cholinergic preponderance in cardiac dynamics (especially
prolongation of the Isometric period of the left ventricle).
The findings obtained in 16 non-cardiac patients concerning the length
of the isometric or tension period (TP), heart rate and pulse pressure
are represented in Table 1.
In response to transthoracic sympathectomy, all three parameters
varied from person to person in wide ranges in both directions. However,
when the tests were repeated in the same patients at different time inter-
vals after the operation (with or without a second contralateral syrn-
pathectomy inbetween), their qualitative pattern of response (either
upward or downward) remained the same in nearly all instances, as
far as the TP and pulse pressure were concerned. The responses of the
heart rate, on the other hand, were less striking percentage-wise and
varied in quite an irregular fashion in identical individuals.
No significant relationship existed between the magnitude of the pre-
operative average values and the type (positive or negative) or degree
of the postoperative deviations in either one of the three recorded pa-
rameters.
DOI 10.1378/chest.38.4.423
1960;38;423-428
Dis Chest
W. RAAB, E. KUX and H. MARCHET
Effect of Transthoracic Endoscopic Sympathectomy
on the Cardiac Neurovegetative Equilibrium
and on Angina Pectoris
We have not found any improvement in ulcer healing with sympathectomy as compared with local wound care and have not performed upper extremity sympathectomy for upper extremity ischemia in over a decade.
Noninvasive Vascular Diagnosis:
A Practical Guide to Therapy
By Ali F. AbuRahma, John J. Bergan
2nd ed., 2007
ISBN: 978-1-84628-446-5
CUTANEOUS INNERVATION IN MAN BEFORE AND AFTER LUMBAR SYMPATHECTOMY: EVIDENCE FOR INTERRUPTION OF BOTH SENSORY AND VASOMOTOR NERVE FIBRES.
ANZ Journal of Surgery. 73(1-2):14-18, January 2003.
COVENTRY, BRENDON J. BM BS, PhD, FRACS *; WALSH, JOHN A. MD, FRACS +
The protein constituents in parasympathetically evoked saliva from normal and short-term sympathectomized parotid glands were compared. There was a reduction in all proline-rich proteins (PRP) in the saliva following sympathectomy. The decrease was quantified for acidic PRP by high-performance ion-exchange chromatography, which showed an increase in the ratio of amylase to other proteins. These results suggest that sympathetic impulses influence the synthesis of PRP and amylase in opposite directions.
http://ep.physoc.org/content/73/1/139.abstract
In conclusion, we showed that sympathectomy produces complex alterations of vascular reactivity both
in vivo and in isolated vessels, which shift the balance of the sensitivity of the vessel between vasoconstrictor and vasodilating agents towards an increased constriction. These results are unlikely to simply reflect denervation supersensitivity; their underlying receptor, post-receptor and/or contractile mechanisms are yet to be identified.
Journal of Hypertension:
August 2000 - Volume 18 - Issue 8 - p 1041-1049
Normal inhibitory influences on pain during sympathetic arousal are compromised in the majority of patients with CRPS. The augmented vasoconstrictor response in the symptomatic limb during sympathetic arousal is consistent with adrenergic supersensitivity. An adrenergic sensitivity in nociceptive afferents might contribute to pain and hyperalgesia during sympathetic arousal in certain patients with CRPS.
Drummond PD,
Finch PM,
Skipworth S,
Blockey P.
School of Psychology, Murdoch University, Perth, Western Australia. drummond@central.murdoch.edu.au
PMID: 11591852 [PubMed - indexed for MEDLINE
These findings suggest that stimuli arousing sympathetic activity act by a central process to exacerbate pain in some patients, independent of the peripheral sympathetic nervous system. This may account for the lack of effect of peripheral sympathetic blockade on pain in some CRPS patients.
Drummond PD,
Finch PM. School of Psychology, Murdoch University, Perth, Western Australia,
PMID: 14707316 [PubMed - indexed for MEDLINE
We report on the ability of a delayed sympathectomy after a prolonged hyperalgesia to result in a subsequent enhanced hyperalgesic response. Sympathectomy was performed one day after injection of prostaglandin E2 plus rolipram, which induces a prolonged sympathetically-maintained hyperalgesia [Aley K. O. and Levine J. D. (1995) Eur. J. Pharmac. 273, 107-112].
http://cat.inist.fr/?aModele=afficheN&cpsidt=3017786
Frontiers in Bioscience 11, 2179-2192, September 1, 2006
Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection.
Annals of the Rheumatic Diseases 1994;53:309-314
http://ard.bmj.com/cgi/content/abstract/53/5/309 In general, enhancing the sympathetic tone decreases both T0-cell and NK cell functions but not the proliferation of splenic B cells (Dowdell and Whitacre, 2000). In contrast, chemical sympathectomy, although having varying results, does seem to increase the severity of autoimmune disorders (Dowdell and Whitacre, 2000)
As far as metabolism, catecholamines promote mobilization of fuel stores at time of stress and act synergistically with glucocorticoids to increased glycogenolysis, gluconeogenesis, and lipolysis but exert opposing effects of protein catabolism, as noted earlier. One important aspect is regulation of body temperature (Goldsttein and Eisenhofer, 2000) Epinephrine levels are also positively related to serum levels of HDL cholesterol and negatively related to triglycerines. However, perturbing the balance of activity of various mediators or metabolism and body weight regulation can lead to well-known metabolic disorders such as type 2 diabetes and obesity.
At the same time, increased sympathetic activitation and nerephinephrine release is elevated in hypertensive individuals and also higher levels of insulin, and there are indications that insulin further increases sympathetic activity in a vicious cycle (Arauz-Pacheco et al.,1996)
As a result of either local production, cytokines often enter the the circultion and can be detected in plasma samples. Sleep deprivation and psychological stress, such as public speaking, are reported to elevate inflammatory cytokine level in blood (Altemus et al., 2001) Circulting levels of a number of inflammatory cytokines are elevated in relation to viral and other infections and contirbute to the feeling of being sick, as well as sleepiness, wiht both direct and indirect effects on the central nervous system (Arkins et al., 2000; Obal and Kueger, 2000)
Inflammatory autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and type 1 diabetes, reflect an allostatic state that consists of at least three principal causes: genetic risk factors, (...) factors that contribute to the development of tolerance of self-antigens (...) and the hormonal mikieu that regulates adaptive immunes responses (Dowdell and Whitacre, 2000)
Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axis hormones, the autonomic nervous system, cytokines, or a number of other systems, and is generally adaptive in the short term [1]
Sympathetic denervation is frequently observed in heart disease. To investigate the linkage of sympathetic denervation and cardiac arrhythmia, we developed a rat model of chemical sympathectomy by subcutaneous injections of 6-hydroxydopamine (6-OHDA).
We observed that sympathectomy (i) decreased cardiac sympathetic nerve density and norepinephrine level, (ii) reduced the protein expression of Kv4.2, Kv1.4, and Kv channel-interacting protein 2 (KChIP2), (iii) decreased current densities and delayed activation of Ito channels, (iv) reduced the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and cAMP response element-binding protein (CREB), and (v) increased the severity of ventricular fibrillation induced by rapid pacing.
We conclude that chemical sympathectomy downregulates the expression of selective Kv channel subunits and decreases myocardial Ito channel activities, contributing to the elevated susceptibility to ventricular fibrillation.
Can. J. Physiol. Pharmacol. 86(10): 700–709 (2008)
Bacq (1931) found that bilateral lumbar sympathectomy in rabbits resulted in sterility with prolonged copulation and absence of orgasm.
J. Reprod. Fertil. (1964) 7, 113-122
The subject has recently been studied by James, Millar&Purves who measured the cerebral vascular response to hypoxia with all nerves intact and following division or stimulation of the vagus and cervical sympathetic nerves. The effect of sympathectomy (...) is seen to consist of an elevation of both grey and white matter blood flow 40-50 per cent above control over the range of PaO2 tested, 35 to 440 mmHg. When the cervical sympathetic nerve as stimulated at constant frequency and intensity, cortical flow was reduced to control levels.
The Physiology of the Cerebral Circulation (Monographs of the Physiological Society) by M. J. Purves (Hardcover - May 31, 1972) Diminished sympathetic constrictor discharge to pulmonary arterioles probably contributes to the lowering of resistance. No direct evidence for such an action has been presented, but the decrease in resting pulmonary resistance that follows thoracic thoracic sympathectomy shows that the potential for such a response exists. Whatever the mechanism, the net result is that pulmonary blood flow can be increased greatly without raising intravascular pressures to a degree that would encourage capillary transudation of fluid.
Cardiovascular physiology
By William R. Milnor
| New York : Oxford University Press, 1990. |
Adoptive transfer experiments indicate that enhanced CD8
+ responses do not result from permanent alterations in CD8
+ T cell function in sympathectomized mice. Rather, additional findings suggest that the sympathetic nervous system tempers the capacity of antigen-presenting cells to activate naïve CD8
+ T cells. We also show that antiviral CD8
+ T cell responses are enhanced by administration of a β
2 (but not β
1 or α) adrenergic antagonist. These findings demonstrate a critical role for the sympathetic nervous system in limiting CD8
+ T cell responses and indicate that CD8
+ T cell responses may be altered in patients using β-blockers, one of the most widely prescribed classes of drugs.
PNAS March 31, 2009 vol. 106 no. 13 Following sympathectomy: (i) the basal t-PA activity in plasma was 70% less than controls (2.92 ± 1.96 versus 9.33 ± 1.72 IU/ml;
P ≤ 0.001); (ii) the acute release from isolated vessels induced by bradykinin or phenylephrine was comparably reduced; and (iii) the greatest reductions occurred in densely innervated small vessel explants. The results provide new support for an autonomic regulation of neural t-PA release into the vessel wall matrix and blood of densely innervated thin-walled microvessels.
Blood Coagulation & Fibrinolysis:
September 2002 - Volume 13 - Issue 6 - pp 471-481
Relationship Between the Vegetative Innervation and the Sensibility of the Nasal MucosaZ. Krajina; Z. Poljak Acta Oto-Laryngologica, 1651-2251, Volume 79, Issue 3, 1975, Pages 172 – 175
This loss of granules is considered to be due to sympathetic "degeneration secretion" caused by the release of noradrenaline from the degenerating adrenergic nerves between 12 and 24 hours after ganglionectomy. This is thought to be the first example of morphological change resulting from "degeneration activation" to be recorded microscopically.
Cell Tissue Res. 1975 Sep 16;162(1):1-12. PMID: 1175216 [PubMed - indexed for MEDLINE]
LERNER
Arch Dermatol.1966; 93: 235-236.
Chronic bilateral postganglionic sympathectomy (4-6 weeks duration) caused a drastic reduction in the capacity of the gland to secrete saliva in response to parasympathetic stimulation, reaching only one-third of that from normal animals. The initial output of amylase was greater than in normal animals but the total output was similar. The control unstimulated sympathectomized glands appeared similar morphologically to normal resting glands. However, on the parasympathetically stimulated side, besides the usual amount of acinar degranulation, there was also a conspicuous development of acinar vacuolation, not seen in the other groups of animals.
J. Physiol. November 15, 2008 586:5537-5547 To examine the effects of cervical sympathectomy on the transport of gonadotropin-releasing hormone (GnRH) between the hypothalamic neurons and the median eminence, 16 male rats were assigned into four groups: control (C), light (L), light-sympathectomy (LS), and light-colchicine (LC).
Considering the action of colchicine, which inhibits axonal transport, it is suggested that cervical sympathectomy also inhibits axonal transports of GnRH between the GnRH neurons and the median eminence during continuous exposure to light.
Journal of AnesthesiaVolume 10, Number 3 / September, 1996 Am J Physiol Heart Circ Physiol 289: H1169-H1175, 2005.
Sympathectomized rats displayed reductions in blood pressure (BP) and atria norepinephrine levels, whereas NGF levels in the DRG, spleen, and ventricles were increased. Sympathectomy also enhanced CGRP and SP mRNA and peptide content in DRG. Administration of CGRP and SP receptor antagonists increased the BP in sympathectomized rats but not in the controls. Thus sympathectomy enhances sensory neuron CGRP and SP expression that contributes to the BP reduction.
http://www.ncbi.nlm.nih.gov/pubmed/1723182?dopt=Abstract
Neuroscience. 1991;45(3):761-5.
Neonatal guanethidine sympathectomy caused an 86% depletion of noradrenaline in the paw skin and neurogenic plasma protein extravasation upon antidromic nerve stimulation was impaired. Sensory neuropeptides were unchanged in the skin after neonatal guanethidine and only calcitonin gene-related peptide content was increased in the spinal cord and sciatic nerves. The other observations (i.e. the sensitivity towards heat stimuli, the neurogenic mustard oil inflammation and the non-neurogenic carrageenan oedema) were similar to those observed after neonatal 6-hydroxydopamine treatment.
The results are consistent with the hypothesis that withdrawal of sympathetic activity is a contributing factor or a prerequisite condition for development of a WAP.(withdrawal-induced antihypertensive phenomenon)
AJP - Heart and Circulatory Physiology, Vol 268, Issue 1 1-H6, Copyright © 1995 by American Physiological Society
The occurrence of receptor binding sites for natriuretic peptides was examined by in vitro receptor autoradiography. In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers. Interestingly, this was found in parallel with a significant decrease of systolic and diastolic blood pressure and increased plasma levels of pro-atrial natriuretic peptide in the treated group of rats. These findings, together with those in previous studies, give support to an idea that one part of the blood pressure-decreasing effects, seen in patients treated with β-adrenergic blockade, might be through a reduction of the natriuretic clearance receptor C, then giving rise to increased levels of atrial natriuretic peptide.
http://cat.inist.fr/?aModele=afficheN&cpsidt=17030448
The recording of sympathetic skin responses (SSRs) is a simple, electrophysiological method to assess sympathetic nerve function. Within the last 10 years, SSRs have mainly been applied to delineate peripheral and central nervous system diseases, although the sympathetic nature of these responses was not fully documented, e.g., by a study of sympathectomy. We therefore recorded SSRs before and after 30 cases of endoscopic thoracic sympathectomy. The main indication was palmar hyperhidrosis, in which we found two types of SSR abnormalities. Most patients exhibited normal SSR waveforms but with increased amplitudes. The other patients exhibited abnormal SSRs which did not occur as single responses but as several consecutive waves.
Published Online: 7 Dec 1998
This study describes the ultrastructural changes in the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis)
after right cervical sympathectomy. Obvious changes in the nodal cells were seen one day after operation. Numerous glycogen particles grouped together to form electron-dense patches containing vacuoles in the cytoplasm. At three days after operation, intracellular organelles exhibited fragmentation and dissolution. By five and seven days after operation, the affected cells were vacuolated and some were swollen and appeared to have degenerated. Simultaneously, there was massive infiltration of macrophages were present nodal tissues. Axon profiles and terminals showing various degrees of degeneration were present in the vicinity of the nodal cells throughout the period of study.
J Anat. 1984 October; 139(Pt 3): 449–461.
Chemical sympathectomy was obtained following intravenous injection of 50 mg·kg–1 of 6-hydroxydopamine. Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.
Cardiovascular Research 1982 16(9):524-529; doi:10.1093/cvr/16.9.524
Patients should be informed of the exercise bradycardia resulting from ISS.
Eur J Cardiothorac Surg 2001;20:1095-1100
Journal of Neurophysiology, Vol 75, Issue 1 514-517, Copyright © 1996 by APS
The induction of adrenergic excitability in CPMs by sympathectomy is suggested to be a counterpart to postsympathectomy neuralgia in human beings and a possible part of the mechanism leading to sympathetically related pain states.
PMID: 9799658 [PubMed - indexed for MEDLINE]
J Mol Cell Cardiol. 1998 Oct;30(10):2047-57. When a nerve is cut, the piece of nerve that is beyond the cut point eventually dies, however, its Schwann cells, the cells that encircle the nerve fibers remain for a much longer time. These Schwann cells secrete a chemical messenger known as nerve growth factor that tells the cut end of nerve where to grow back. So the cut end of nerve will send out multiple sprouts in the direction of the nerve growth factor, however, these sprouts do not go out in an orderly manner, instead they grow out in all directions and eventually cluster and form a knot of nerve fibers. This eventually leads to the formation of a TRUE neuroma or a END BULB or STUMP neuroma.
www.tarsaltunnelcenter.com/assets/recurrent.shtml Even epidural blockade limited only to the thoracic dermatomes is liable to cause complete sympathectomy, including cardiac sympathetic denervation. The ensuing vasodilation and bradycardia lead to hypotension, poor tolerance of mechanical interference with the heart, and inability to respond to acute changes in intravascular volume or body position. This symptom complex is especially troublesome to manage during intrathoracic operations when avoidance of hypervolemia is emphasized.
Thoracic sympathectomy has two other potenital consequences: effect on bronchomotor tone and effect on oxygenation.
During intrathoracic procedures using one-lung ventilation, a right-to-left intrapulmonary shunt is intentionally created (in the form of the nonventilated lung). The ensuing arterial oxygen tension (PaO2) is determined by a complex interaction involving cardiac output, mixed venous oxygen tension, the status of the ventilated lung, size of the shunt, and most significantly, hypoxic pulmonary vasoconstriction (HPV).
HPV diverts pulmonary blood flow away from the shunt by vavsoconstriction in the nonventilated lung, and is the principal adaptive defense mechanism against arterial hypoxemia during one-lung ventilation. The cellular mechanism and regulation of HPV, and the possible role of the autonomic nervous system are not completely understood.
The effect of thoracic sympathectomy of HPV is even less well understood. Since potent vasodilators such as nitroprusside antagonize HPV-induced vasoconstriction and lower the arterial oxygen tension, it is reasonable to assume that HPVwill become less effective with thoracic sympathectomy.
Clinical studies have produced conflicting conclusions, most probably because direct measurement of HPV is not possible in human studies, and the surrogate endpoing examined PaO2 is determined not only by HPV, but also by a host of interacting factors, some of which may be affected by the sympathectomy and can not be held constant.
Risk Factor for Neuraxial Anesthesia-Associated Bradycardia:
Block height higher than T5
Younger age
Publication Date: 2007-01-01 Publisher: MCGRAW-HILL EDUCATION - EUROPE Country of origin: UNITED STATES
Jeng and associates observed an increase in cerebral blood flow after T2 sympathectomy, and they suggested the possibility of using such a surgical approach to improve cerebral blood flow in patients with cerebral vascular insufficiency.
Youmans Neurological Surgery, 5th Edition
Publisher: Saunders
Publication Date: 2003-10-10
In the 1930's it was recognised by neurosurgeons performing destructive sympathectomies for angina pectoris that local anaesthetic infiltration around the stellate ganglion often resulted in pain relief outlasting the duration of action of the local anaesthetic drug
13. This observation has been more recently confirmed
14, and is currently (June 1999) the subject of a large scale randomised double-blind placebo-controlled trial funded by the British Heart Foundation.
The pathogenesis of angina and myocardial infarction pain involves the activation of the afferent sympathetic pathway. A frequent and important consequence of pain (especially when severe) is the `flight or fight' response through activation of sympathetic efferents. The clinical image of the patient with an acute myocardial infarction (cold, clammy, sweaty, anxious, tachycardic) is secondary to this adrenergic activation. Therefore, angina might be regarded as the sensory component of a positive feedback loop, which cannot under these circumstances be conceived as resulting in benefit, and which may be considered to be a maladaption.
The angina-relieving effects of sympathetic blockade might be due to interference with this maladaptive feedback loop, in a similar manner to the way in which adenosine interrupts a re-entrant tachycardia. If such a loop exists, it may partly explain chronic refractory angina and the fact that temporary interruption of this pathway has a prolonged effect on pain14. Beneficial amelioration of angina can be achieved with repeated blocks14. There does not appear to be any predictability in the length of time a patient remains pain-free after successive blocks.
http://www.angina.org/source/pro/symp_block.htm
Six experiments are reported on the effects of 2,4,5-trihydroxyphenylethyl-amine (6-hydroxydopamine) on two-way escape and avoidance learning. Rats were tested on either escape or avoidance learning at 80 days of age after chemical sympathectomy at birth or 40 or 80 days of age. Neonatal and chronic sympathectomy (at 40 days), but not acute sympathectomy (at 80 days), resulted in depressed escape learning. Avoidance learning was affected by neonatal sympathectomy and partially by acute sympathectomy. The results have implications for the role of the autonomic nervous system in escape-avoidance learning.
J Comp Physiol Psychol 1976; 90:303-16.
Acta Otolaryngol. 1978 Nov-Dec;86(5-6):314-30.
PMID: 213930 [PubMed - indexed for MEDLINE]
It is proposed that the autonomic innervation of brain vessels participates in the control not only of the cerebral circulation but also of associated intracranial pressure phenomena.
Blood Vessels 1974;11:2-31
Moya-Moya Syndrome
Moya Moya syndrome is a vasculopathy of the cranial arteries, usually the carotids, leading to progressive intracranial occlusion with distal collateral vessels. This is a very frequent cause of pediatric stroke in India(10,11). Children usually present with an acute focal deficit such as hemiplegia, whereas in later years sub-arachnoid hemorrhage is a common presenta-tion. Due to bilateral carotid involvement sometimes alternating hemiplegia is seen. The outcome varies widely without treatment. Moya Moya disease is usually idiopathic, although same radiographic pattern is seen in some patients with sickle cell disease, neuro-fibromatosis, postcranial irradiation and in various other conditions(15). There is no proven treatment of Moya Moya disease. Medical management involves use of aspirin but needs further testing. Surgical treatment involves cervical sympathectomy, intracranial graft of omentum or temporalis muscle and bypass of superficial temporal artery to the middle cerebral artery(34).
http://indianpediatrics.net/feb2000/personal.htm
In conscious animals, cervical sympathectomy greatly reduces ventilation in normoxia and slightly affects ventilatory responses to hypoxia and hypercapnia, also suggesting an important role for these nerves in the control of breathing.
Eur Respir J 1998; 12: 177–184
Cervical sympathectomy
A form of surgery that is useful for some people with LQTS. It reduces the amount of adrenaline and its by-products produced and delivered to the heart by certain nerves (the left cervical ganglia). It involves operating on the left neck and removing or blocking these nerves
http://www.sads.org.uk/technical_terms.htm
We conclude that adrenalectomy near-totally
ablates the hypothermia-associated increase in RSCBF measured in intact
rats and that abdominal sympathectomy totally ablates it. This evidence
complements morphological evidence for adrenergic innervation of the spinal
cord vasculature.
http://ajpheart.physiology.org/cgi/content/abstract/260/3/H827
Transverse myelitis
Transverse myelitis is a
neurological disorder caused by an
inflammatory process of the
grey and
white matter of the
spinal cord, and can cause
axonal demyelination.
In some cases, the disease is presumed to be caused by viral infections or vaccinations and has also been associated with spinal cord injuries, immune reactions,
schistosomiasis and
insufficient blood flow through spinal cord vessels. Acute myelitis accounts for 4 to 5 percent of all cases of
neuroborreliosis.
[1] Symptoms include weakness and numbness of the limbs as well as motor, sensory, and sphincter deficits. Severe backpain may occur in some patients at the onset of the disease.
http://en.wikipedia.org/wiki/Transverse_myelitis
